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==Treatment== There are many causes of necrosis, and as such treatment is based upon how the necrosis came about. Treatment of necrosis typically involves two distinct processes: Usually, the underlying cause of the necrosis must be treated before the dead tissue itself can be dealt with.{{citation needed|date=June 2022}} * [[Debridement]], referring to the removal of dead tissue by surgical or non-surgical means, is the standard therapy for necrosis. Depending on the severity of the necrosis, this may range from removal of small patches of skin to complete [[amputation]] of affected limbs or organs. Chemical removal of necrotic tissue is another option in which enzymatic debriding agents, categorised as [[proteolytic]], [[fibrinolytic]] or [[collagenase]]s, are used to target the various components of dead tissue.<ref name="Anu">{{cite journal | vauthors = Singhal A, Reis ED, Kerstein MD | title = Options for nonsurgical debridement of necrotic wounds | journal = Advances in Skin & Wound Care | volume = 14 | issue = 2 | pages = 96β100; quiz 102β3 | year = 2001 | pmid = 11899913 | doi = 10.1097/00129334-200103000-00014 }}</ref> In select cases, special [[maggot therapy]] using ''[[Lucilia sericata]]'' larvae has been employed to remove necrotic tissue and infection.<ref name="Horobin">{{cite journal | vauthors = Horobin AJ, Shakesheff KM, Pritchard DI | title = Maggots and wound healing: an investigation of the effects of secretions from Lucilia sericata larvae upon the migration of human dermal fibroblasts over a fibronectin-coated surface | journal = Wound Repair and Regeneration | volume = 13 | issue = 4 | pages = 422β433 | year = 2005 | pmid = 16008732 | doi = 10.1111/j.1067-1927.2005.130410.x | s2cid = 7861732 }}</ref> * In the case of [[ischemia]], which includes [[myocardial infarction]], the restriction of blood supply to tissues causes [[Hypoxia (medical)|hypoxia]] and the creation of [[reactive oxygen species]] (ROS) that react with, and damage proteins and membranes. [[Antioxidant]] treatments can be applied to scavenge the ROS.<ref name="Eum">{{cite journal | vauthors = Eum HA, Cha YN, Lee SM | title = Necrosis and apoptosis: sequence of liver damage following reperfusion after 60 min ischemia in rats | journal = Biochemical and Biophysical Research Communications | volume = 358 | issue = 2 | pages = 500β5 | date = June 2007 | pmid = 17490613 | doi = 10.1016/j.bbrc.2007.04.153 }}</ref> * Wounds caused by physical agents, including physical [[Trauma (medicine)|trauma]] and [[chemical burns]], can be treated with [[antibiotics]] and [[anti-inflammatory]] drugs to prevent bacterial infection and inflammation. Keeping the wound clean from infection also prevents necrosis. * Chemical and toxic agents (e.g. pharmaceutical drugs, acids, bases) react with the skin leading to skin loss and eventually necrosis. Treatment involves identification and discontinuation of the harmful agent, followed by treatment of the wound, including prevention of infection and possibly the use of [[immunosuppressive]] therapies such as [[anti-inflammatory drugs]] or immunosuppressants.<ref name="Cooper">{{cite journal | vauthors = Cooper KL | title = Drug reaction, skin care, skin loss | journal = Critical Care Nurse | volume = 32 | issue = 4 | pages = 52β59 | date = August 2012 | pmid = 22855079 | doi = 10.4037/ccn2012340 | doi-access = free }}</ref> In the example of a [[snake bite]], the use of [[anti-venom]] halts the spread of toxins whilst receiving [[antibiotics]] to impede infection.<ref name="Chrotenimitkhum">{{cite journal | vauthors = Chotenimitkhun R, Rojnuckarin P | title = Systemic antivenom and skin necrosis after green pit viper bites | journal = Clinical Toxicology | volume = 46 | issue = 2 | pages = 122β5 | date = February 2008 | pmid = 18259959 | doi = 10.1080/15563650701266826 | s2cid = 6827421 }}</ref> Even after the initial cause of the necrosis has been halted, the necrotic tissue will remain in the body. The body's immune response to apoptosis, which involves the automatic breaking down and recycling of cellular material, is not triggered by necrotic cell death due to the apoptotic pathway being disabled.<ref name="Edinger">{{cite journal | vauthors = Edinger AL, Thompson CB | title = Death by design: apoptosis, necrosis and autophagy | journal = Current Opinion in Cell Biology | volume = 16 | issue = 6 | pages = 663β9 | date = December 2004 | pmid = 15530778 | doi = 10.1016/j.ceb.2004.09.011 }}</ref>
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